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Renoprotective effects of apocynin and/or umbelliferone against acrylamide-induced acute kidney injury in rats: role of the NLRP3 inflammasome and Nrf-2/HO-1 signaling pathways.
Ageena, Saad A; Bakr, Adel G; Mokhlis, Hamada A; Abd-Ellah, Mohamed F.
Afiliación
  • Ageena SA; Department of Pharmacology & Toxicology, Faculty of Pharmacy, Al Azhar University, Assiut Branch, Assiut, 71524, Egypt. saadageena.2045@azhar.edu.eg.
  • Bakr AG; Department of Pharmacology & Toxicology, Faculty of Pharmacy, Al Azhar University, Assiut Branch, Assiut, 71524, Egypt.
  • Mokhlis HA; Department of Pharmacology & Toxicology, Faculty of Pharmacy (Boys), Al-Azhar University, Cairo, Egypt.
  • Abd-Ellah MF; Department of Pharmacy Practice, Faculty of Pharmacy, Kantara Branch, Sinai University, Cairo, Egypt.
Naunyn Schmiedebergs Arch Pharmacol ; 2024 Jul 19.
Article en En | MEDLINE | ID: mdl-39028331
ABSTRACT
Acrylamide (ACR) is a toxic, probably carcinogenic compound commonly found in fried foods and used in the production of many industrial consumer products. ACR-induced acute kidney injury is mediated through several signals. In this research, we investigated, for the first time, the therapeutic effects of phytochemicals apocynin (APO) and/or umbelliferone (UMB) against ACR-induced nephrotoxicity in rats and emphasized the underlying molecular mechanism. To achieve this goal, five groups of rats were randomly assigned the control group received vehicle (0.5% CMC; 1 ml/rat), ACR (40 mg/kg, i.p.), ACR + APO (100 mg/kg, P.O.), ACR + UMB (50 mg/kg, P.O.), and combination group for 10 days. In ACR-intoxicated rats, there was a significant reduction in weight gain while the levels of blood urea, uric acid, creatinine, and Kim-1 were elevated, indicating renal injury. Histopathological injury was also observed in the kidneys of ACR-intoxicated rats, confirming the biochemical data. Moreover, MDA, TNF-α, and IL-1ß levels were raised; and GSH and SOD levels were decreased. In contrast, treatment with APO, UMB, and their combination significantly reduced the kidney function biomarkers, prevented tissue damage, and decreased inflammatory cytokines and MDA. Mechanistically, it suppressed the expression of NLRP-3, ASC, GSDMD, caspase-1, and IL-1ß, while it upregulated Nrf-2 and HO-1 in the kidneys of ACR-intoxicated rats. In conclusion, APO, UMB, and their combination prevented ACR-induced nephrotoxicity in rats by attenuating oxidative injury and inflammation, suppressing NLRP-3 inflammasome signaling, enhancing antioxidants, and upregulating Nrf-2 and HO-1 in the kidneys of ACR-induced rats.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Naunyn Schmiedebergs Arch Pharmacol Año: 2024 Tipo del documento: Article País de afiliación: Egipto Pais de publicación: Alemania
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Naunyn Schmiedebergs Arch Pharmacol Año: 2024 Tipo del documento: Article País de afiliación: Egipto Pais de publicación: Alemania